Ductal metaplasia in pancreas

Pancreatic ductal metaplasia (PDM) is the transformation of potentially many type of cells in pancreas into ductal or ductal-like cells, which eventually replace the existing differentiated somatic cell type(s). PDM is usually triggered by and manifests its ability to adapt to environmental and cellular stimuli and stresses. Acinar to ductal metaplasia (ADM) is the predominant form of ductal metaplasia in pancreas. The cellular heterogeneity of PDM informs the differences in cellular origin, triggering events, functional subpopulations and evolution pathways of PDM. Currently it remains uncertain what are the exact cellular origins and functional significance of PDM, and how this process is regulated at cellular and molecular levels. The development of PDM to atypical hyperplasia is an important risk factor for pancreatic precursors, including intraepithelial neoplasia (PanIN), and pancreatic ductal adenocarcinoma (PDAC). Otherwise, the cellular plasticity in PDM contribute to the regeneration of both exocrine and endocrine components of pancreas. This Review will systematically describe current knowledge on the understanding of PDM biology with an emphasis on its underlying mechanisms and implications in pancreatic regeneration, inflammation and tumorigenesis.

Automated summary

Pancreatic ductal metaplasia (PDM) is the process where various types of cells in the pancreas transform into ductal or ductal-like cells. The exact cellular origins and functional significance of PDM, as well as its cellular and molecular regulation, are still uncertain. PDM development is associated with increased risk of pancreatic precursors and pancreatic ductal adenocarcinoma, while cellular plasticity in PDM contributes to the regeneration of pancreatic tissue.